Links the remodeling process with the biosynthesis of mediators of inflammation and diseases
Provides a new perspective by following the movement of the substrate (AA) rather than discussing single enzymes and their related mediators
International authorship
Arachidonic acid (AA) and other 20 or 22-carbon polyunsaturated fatty acids (PUFAs) are precursors of lipid mediators of inflammation known as eicosanoids. These mediators are critical in disease processes and in regulating normal cell function. Remodeling is important in maintaining homeostasis and in regulating cell function by dictating how PUFAs are converted to lipid mediators of inflammation. Thus, PUFA remodeling is a critical process in the biosynthesis of a multitude of mediators, and understanding this process will unravel better therapeutic targets for controlling inflammatory diseases such as asthma and Alzheimer´s disease.
AA metabolism is described in an integrated context linking the remodeling processes with the biosynthesis of mediators and diseases. By following the movement of the substrate (AA), the volume describes how upstream biosynthetic pathways influence the formation of lipid mediators of inflammation, showing the metabolic interrelationship between all AA-derived mediators.
An outline of arachidonate remodeling and its biological significance.- Phospholipase A2 and remodeling in inflammatory cells.- Enzymatic and receptor mediated effects of secretory phospholipase A2 on the pathophysiology of inflammatory diseases.- Control of arachidonic acid levels in resting and activated U937 phagocytic cells by Ca2+-independent phospholipase A2.- Arachidonate remodeling and PAF synthesis in human neutrophils.- Control of long chain polyunsaturated fatty acid levels and the role of inhibitors of incorporation and remodeling on the biosynthesis of lipid mediators.- Remodeling of arachidonic acid in inflammatory cells of the human lung.- Arachidonate remodeling, platelet-activating factor signaling, and the inflammatory response in the central nervous system.- Remodeling of arachidonate and other polyunsaturated fatty acids in Alzheimer´s disease.- Lipoxins and resolvins: local mediators in endogenous anti-inflammation and resolution.- Metabolism and physiological significance of anandamide and 2-arachidonoylglycerol, endogenous cannabinoid receptor ligands.
Arachidonic acid (AA) and other 20 or 22-carbon polyunsaturated fatty acids (PUFAs) are precursors of lipid mediators of inflammation known as eicosanoids. These mediators are critical in disease processes and in regulating normal cell function. Remodeling is important in maintaining homeostasis and in regulating cell function by dictating how PUFAs are converted to lipid mediators of inflammation. Thus, PUFA remodeling is a critical process in the biosynthesis of a multitude of mediators, and understanding this process will unravel better therapeutic targets for controlling inflammatory diseases such as asthma and Alzheimer's disease.
AA metabolism is described in an integrated context linking the remodeling processes with the biosynthesis of mediators and diseases. By following the movement of the substrate (AA), the volume describes how upstream biosynthetic pathways influence the formation of lipid mediators of inflammation, showing the metabolic interrelationship between all AA-derived mediators.
An outline of arachidonate remodeling and its biological significance.- Phospholipase A2 and remodeling in inflammatory cells.- Enzymatic and receptor mediated effects of secretory phospholipase A2 on the pathophysiology of inflammatory diseases.- Control of arachidonic acid levels in resting and activated U937 phagocytic cells by Ca2+-independent phospholipase A2.- Arachidonate remodeling and PAF synthesis in human neutrophils.- Control of long chain polyunsaturated fatty acid levels and the role of inhibitors of incorporation and remodeling on the biosynthesis of lipid mediators.- Remodeling of arachidonic acid in inflammatory cells of the human lung.- Arachidonate remodeling, platelet-activating factor signaling, and the inflammatory response in the central nervous system.- Remodeling of arachidonate and other polyunsaturated fatty acids in Alzheimer's disease.- Lipoxins and resolvins: local mediators in endogenous anti-inflammation and resolution.- Metabolism and physiological significance of anandamide and 2-arachidonoylglycerol, endogenous cannabinoid receptor ligands.
Inhaltsverzeichnis
An outline of arachidonate remodeling and its biological significance.- Phospholipase A2 and remodeling in inflammatory cells.- Enzymatic and receptor mediated effects of secretory phospholipase A2 on the pathophysiology of inflammatory diseases.- Control of arachidonic acid levels in resting and activated U937 phagocytic cells by Ca2+-independent phospholipase A2.- Arachidonate remodeling and PAF synthesis in human neutrophils.- Control of long chain polyunsaturated fatty acid levels and the role of inhibitors of incorporation and remodeling on the biosynthesis of lipid mediators.- Remodeling of arachidonic acid in inflammatory cells of the human lung.- Arachidonate remodeling, platelet-activating factor signaling, and the inflammatory response in the central nervous system.- Remodeling of arachidonate and other polyunsaturated fatty acids in Alzheimer's disease.- Lipoxins and resolvins: local mediators in endogenous anti-inflammation and resolution.- Metabolism and physiological significance of anandamide and 2-arachidonoylglycerol, endogenous cannabinoid receptor ligands.
Arachidonic acid (AA) and other 20 or 22-carbon polyunsaturated fatty acids (PUFAs) are precursors of lipid mediators of inflammation known as eicosanoids. These mediators are critical in disease processes and in regulating normal cell function. Remodeling is important in maintaining homeostasis and in regulating cell function by dictating how PUFAs are converted to lipid mediators of inflammation. Thus, PUFA remodeling is a critical process in the biosynthesis of a multitude of mediators, and understanding this process will unravel better therapeutic targets for controlling inflammatory diseases such as asthma and Alzheimer's disease.
AA metabolism is described in an integrated context linking the remodeling processes with the biosynthesis of mediators and diseases. By following the movement of the substrate (AA), the volume describes how upstream biosynthetic pathways influence the formation of lipid mediators of inflammation, showing the metabolic interrelationship between all AA-derived mediators.
